The identity and topographic localization of immunocompetent cells and the alteration of surface markers on ocular resident cells in mice and rodents with experimental autoimmune uveoretinitis (EAU) were analyzed by immunohistochemical studies and in situ hybridization. T lymphocytes were the predominantly infiltrating cells in rat EAU, yet both macrophages and T helpers/inducers were the predominantly infiltrating cells in mouse EAU. The migration of inflammatory cells from vessels into target sites is directed by adhesion molecules that can be expressed on vascular endothelium and other resident cells in the eye. T-lymphocyte specificity is directed to small fragments of antigen bound to cell surface major histocompatibility complex (MHC) molecules, which are presented on the surface of specialized antigen-presenting cells. The expression of MHC class II antigens was observed on ocular resident cells such as retinal pigment epithelium (RPE), retinal vascular endothelium, keratocytes, fibroblasts, and ciliary epithelium in rodents. The expression of MHC class II antigens is confined to ocular resident cells immediately at the inflammatory sites in mouse EAU, which is characterized by focal lesions and chronicity. Both the infiltrating cell subpopulation and the expression of class II antigens on ocular resident cells can be altered by various immunomodulating agents. Experimental endotoxin-induced uveitis (EIU) is a model for anterior uveitis in humans. The mechanism of this inflammation is still unclear, although activation of phospholipase A2 (PLA2) may play a role in the initiation and propagation of this disease. The particular vascular structure of the anterior uvea and the role of adhesion molecules (such as intercellular adhesion molecule and endothelial leukocyte adhesion molecule) and their ligand (lymphocyte function-associated antigen) also were examined in EIU and EAU models. Inhibition of PLA2 (chlorpromazine, antiflammin, etc.) and adhesion molecules can abrogate EIU.